The Mouse Snail Gene Encodes a Key Regulator of the Epithelial-Mesenchymal Transition

The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
Molecular and Cellular Biology (Impact Factor: 4.78). 01/2002; 21(23):8184-8. DOI: 10.1128/MCB.21.23.8184-8188.2001
Source: PubMed


Snail family genes encode DNA binding zinc finger proteins that act as transcriptional repressors. Mouse embryos deficient
for the Snail (Sna) gene exhibit defects in the formation of the mesoderm germ layer. In Sna
−/− mutant embryos, a mesoderm layer forms and mesodermal marker genes are induced but the mutant mesoderm is morphologically
abnormal. Lacunae form within the mesoderm layer of the mutant embryos, and cells lining these lacunae retain epithelial characteristics.
These cells resemble a columnar epithelium and have apical-basal polarity, with microvilli along the apical surface and intercellular
electron-dense adhesive junctions that resemble adherens junctions. E-cadherin expression is retained in the mesoderm of the
−/− embryos. These defects are strikingly similar to the gastrulation defects observed insnail-deficient Drosophila embryos, suggesting that the mechanism of repression of E-cadherin transcription by Snail family proteins may have been present
in the metazoan ancestor of the arthropod and mammalian lineages.

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Available from: Rulang Jiang, Jan 06, 2015
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    • "Certain proteins relevant to phenotypic developmental changes in stem cells and transformed cells have been described (Zheng and Kang, 2014). The transcriptional repressor Snail is essential for gastrulation and mesoderm formation during mammalian development (Carver et al., 2001). Snail levels increase in transformed cells. "
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    • "Historically, the Snail family is most well known for roles in embryonic development [14] however, Snail proteins have also been shown to play a prominent role in hematopoiesis [15]. Due to embryonic lethality resulting from germline deletion of Snai1, the hematopoietic functions of this family member have not yet been defined [16] [17]. The germline deletion of Snai2 (g2KO) is viable with piebaldism of variable penetrance [18]. "
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    • "Interestingly, Slug knockout mice are viable with no major phenotype (Jiang et al., 1998), although loss of the closely related gene Snail causes early embryonic lethality due to problems with gastrulation (Carver et al., 2001). It is therefore possible that Snail compensates for the loss of Slug during early development, masking a potential role for Slug in this process. "
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